Linkage of a tumor immune function and cell cycle de-regulation via a gene regulatory network subcircuit.
Gene regulatory network (GRN) subcircuits have been described for cell fate progressions in animal development. The hallmark of these subcircuits is the integration of promoters, and positive- and negative-acting promoter binding proteins, such that an alteration in function of any one member of the defined subcircuit, occurring with a change in cell fate, defines a change in status for all other members of the subcircuit. Here we describe a GRN subcircuit that links a tumor immune function with cell cycle de-regulation. All members of this subcircuit have a predictable status change in response to rescue of the growth-controlled phenotype. Given the similarities between the molecular mechanisms underlying cell status changes in tumorigenesis and development, application of GRN paradigms to tumor progression is particularly apt and offers the hope of providing a more concise, reliable, and therapeutically useful series of predictions linking gene regulation and tumor progression.
Xu
Lijun
L
Department of Molecular Medicine, College of Medicine, University of South Florida, Tampa, FL 33612, USA.
Niesen
Melissa I
MI
Blanck
George
G
D002453:Cell Cycle / Q000235:genetics* / Q000276:immunology; D045744:Cell Line, Tumor; D015972:Gene Expression Regulation, Neoplastic; D053263:Gene Regulatory Networks / Q000235:genetics* / Q000276:immunology; D006801:Humans; D009369:Neoplasms / Q000235:genetics* / Q000276:immunology; D027702:Organic Cation Transporter 1 / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D011401:Promoter Regions, Genetic; D050986:YY1 Transcription Factor / Q000235:genetics* / Q000276:immunology / Q000378:metabolism
D027702:Organic Cation Transporter 1; D050986:YY1 Transcription Factor; C494698:YY1 protein, human